ESR1 gene amplification in endometrial carcinomas: a clinicopathological analysis.
ESR1 gene amplification in endometrial carcinomas: a clinicopathological analysis.
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发表时间：
2013-09
影响因子：
2
通讯作者：
M. T. Rahman;K. Nakayama;Munmun Rahman;M. Ishikawa;H. Katagiri;A. Katagiri;T. Ishibashi;E. Sato;K. Iida;Noriyuki Ishikawa;N. Nakayama;K. Miyazaki
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作者：
M. T. Rahman;K. Nakayama;Munmun Rahman;M. Ishikawa;H. Katagiri;A. Katagiri;T. Ishibashi;E. Sato;K. Iida;Noriyuki Ishikawa;N. Nakayama;K. Miyazaki
本研究探讨了子宫内膜癌中雌激素受体 1 (ESR1) 基因扩增的临床病理意义及其与磷酸酶和张力蛋白同源物 (PTEN)、人表皮生长因子受体 2 (HER2)、MutL 同源物 1 (MLH1)、p53 和富含 AT 相互作用结构域 1A (ARID1A) 表达的关系。通过荧光原位杂交和免疫组织化学评估 ESR1 扩增和表达。通过回顾性图表审查收集临床数据。 111 例子宫内膜癌中有 13 例（11.7%）发现 ESR1 扩增。 ESR1 扩增与国际妇产科联合会 (FIGO) 分期 (p=0.17)、组织学分级 (p=0.35)、淋巴结转移 (p=0.51) 或深肌层浸润 (p=0.46) 之间没有观察到显着关联。 ESR1 扩增独立于 PTEN、p53、HER2、MLH1 和 ARID1A 蛋白表达。没有雌激素受体（ER）或孕激素受体（PR）表达的患者比有ER或PR表达的患者无进展生存期和总生存期更短（p<0.01）。 ESR1 扩增独立于与不良预后和 PTEN、p53、HER2、MLH1 和 ARID1A 蛋白表达相关的已知临床病理因素，表明 ESR1 扩增可能是子宫内膜癌发展的早期事件。
This study investigated the clinicopathological significance of estrogen receptor 1 (ESR1) gene amplification and its relationship to phosphatase and tensin homolog (PTEN), human epidermal growth factor receptor 2 (HER2), MutL homolog 1 (MLH1), p53, and AT rich interactive domain 1A (ARID1A) expression in endometrial carcinomas. ESR1 amplification and expression were assessed by fluorescence in situ hybridization and immunohistochemistry. Clinical data were collected by retrospective chart review. ESR1 amplification was identified in 13 out of 111 (11.7%) endometrial carcinomas. No significant association was observed between ESR1 amplification and International Federation of Gynecology and Obstetrics (FIGO) stage (p=0.17), histological grade (p=0.35), lymph node metastasis (p=0.51), or deep myometrial invasion (p=0.46). ESR1 amplification was independent of PTEN, p53, HER2, MLH1, and ARID1A protein expression. Patients without estrogen receptor (ER) or progesterone receptor (PR) expression had shorter progression-free and overall survival than those with ER or PR expression (p<0.01). ESR1 amplification is independent of known clinicopathological factors related to poor prognosis and PTEN, p53, HER2, MLH1, and ARID1A protein expression, suggesting ESR1 amplification may be an early event in endometrial carcinoma development.